Pregnancy induced hypertension (PIH) complicates 5% of pregnancies and is associated with perinatal and maternal morbidity and mortality. Fetal hypoxia is common but only sporadically responds to reduced vasospasm. An additional mechanism to compound circulatory hypoxia may evolve from the common complication of increased red cell turnover and resultant heme catabolism in PIH. Carbon monoxide (CO) is a catabolic by-product of heme. It alters oxygen transfer as carboxyhemoglobin (COHb), decreasing 02 carrying capacity and causing shift to the left. This project proposes to clarify the relationship between maternal endogenous CO production, 02 transfer and fetal hypoxia. These aims will be met by carefully classifying hypertensive subjects into appropriate clinical groups, compared to normotensive controls. By measuring concurrently for COHb, PO2, 02 content and capacity, and oxyhemoglobin dissociation in fetal, maternal and cord blood, the role of C0 in 02 transfer in PIH will be clarified. By intergroup comparisons, the sensitivity and specificity for PIH will be ascertained, and the impact of covariables such as anemia and smoking determined. Finally, the project will test the hypothesis that maternal hyperoxygenation can effectively reverse this process, displace CO from maternal and fetal hemoglobin, shifting P50 to the right and thus reverse fetal stress/distress.